Hyoung Ja Kim

In our search for bioactive components, various chromatographic separations of the organic fractions from Filipendula glaberrima leaves led to the isolation of a new ellagitannin and a triterpenoid, along with 26 known compounds. The structures of the isolates were determined based on their spectroscopic properties and chemical evidence, which were then evaluated for their antioxidant activities, inhibitory activities on 3-hydroxy-3-methylglutaryl-coenzyme A reductase, and foam cell formation in THP-1 cells to prevent atherosclerosis. Rugosin B methyl ester (1) showed the best HMG-CoA reductase inhibition and significantly reduced ox-low-density lipoprotein-induced THP-1 macrophage-derived foam cell formation at 25 µM. In addition, no cytotoxicity was observed in THP-1 cells at 50 μg/mL of all extracts in the macrophage foam cell formation assay. Therefore, F. glaberrima extract containing 1 is promising in the development of dietary supplements due to its potential behavior as a novel source of nutrients for preventing and treating atherosclerosis.

Trichosanthes kirilowii, one of the herbal formulas named SH003, has been used for treatment in traditional medicine. This paper aimed to analyze the marker compounds from the roots of T. kirilowii and evaluate a validation method for cucurbitacins B and D using high-performance liquid chromatography-photodiode array detector (HPLC-PDA). Two marker compounds were identified as cucurbitacin B (1) and cucurbitacin D (2) from the roots of T. kirilowii by spectroscopic analyses. Cucurbitacins B and D peaks were well separated and were detected at 15.4min and 12.4min, respectively, by a UV detector at 230nm with the linearity (R²>0.999) range between 5 and 250μg/mL, limit of detections (LODs) were 1.87μg/mL and 1.30μg/mL, respectively, while limit of quantifications (LOQs) were 5.66μg/mL and 3.93μg/mL, respectively. The established method offered good precision with overall intra- and inter-day variations of 0.341.26 and 0.261.35, respectively, for relative standard deviation (RSD, acceptance limit RSD B and D recoveries ranged from 99.2 to 101.7 and 98.6 to 102.0, respectively. These results suggest that cucurbitacins B and D could be a valuable candidate for marker compounds of the extract from T. kirilowii, and the proposed method was shown applicability for quality control of SH003.

Aster glehni F. Schmidt (AG), is a natural product known to have anti-obesity effects, but the mechanism underlying these effects is not well documented. We hypothesized that AG may have inhibitory effects on enzymes related to lipid accumulation. Herein, AG fractions were tested against HMG-CoA reductase (HMGR) and fatty acid synthase (FAS), two important enzymes involved in cholesterol and fatty acid synthesis, respectively. We found that dicaffeoylquinic acid (DCQA) methyl esters present in AG are largely responsible for the inhibition of HMGR and FAS. Since free DCQA is a major form present in AG, we demonstrated that a simple methylation of the AG extract could increase the overall inhibitory effects against those enzymes. Through this simple process, we were able to increase the inhibitory effect by 150%. We believe that our processed AG effectively modulates the HMGR and FAS activities, providing promising therapeutic potential for cholesterol- and lipid-lowering effects.

[This corrects the article DOI: 10.1155/2017/3912567.].

Our previous study showed that hydrangenol isolated from Hydrangea serrata leaves exerts antiphotoaging activity in vitro. In this study, we determined its antiphotoaging effect in UVB-irradiated HR-1 hairless mice. We evaluated wrinkle formation, skin thickness, histological characteristics, and mRNA and protein expression using qRT-PCR and Western blot analysis in dorsal skins. Hydrangenol mitigated wrinkle formation, dorsal thickness, dehydration, and collagen degradation. Hydrangenol increased the expression of involucrin, filaggrin, and aquaporin-3 (AQP3) as well as hyaluronic acid (HA) production via hyaluronidase (HYAL)-1/-2 downregulation. Consistent with the recovery of collagen composition, the expression of Pro-COL1A1 was increased by hydrangenol. Matrix metalloproteinase (MMP)-1/-3, cyclooxygenase-2 (COX-2), and interleukin-6 (IL-6) expression was reduced by hydrangenol. Hydrangenol attenuated the phosphorylation of mitogen-activated protein kinases (MAPKs) including ERK and p38, activator protein 1 (AP-1) subunit, and signal transduction and activation of transcription 1 (STAT1). Hydrangenol upregulated the expression of nuclear factor-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO-1), glutamate cysteine ligase modifier subunit (GCLM), and glutamate cysteine ligase catalysis subunit (GCLC). Taken together, our data suggest that hydrangenol can prevent wrinkle formation by reducing MMP and inflammatory cytokine levels and increasing the expression of moisturizing factors and antioxidant genes.

Skin photoaging is mainly caused by exposure to ultraviolet (UV) light, which increases expressions of matrix metalloproteinases (MMPs) and destroys collagen fibers, consequently inducing wrinkle formation. Nutritional factors have received scientific attention for use as agents for normal skin functions. The aim of this study was to investigate the effect of hot water extracts from the leaves of Hydrangea serrata (Thunb.) Ser. (WHS) against ultraviolet B (UVB)-induced skin photoaging and to elucidate the underlying molecular mechanisms in human foreskin fibroblasts (Hs68) and HR-1 hairless mice. WHS recovered UVB-reduced cell viability and ameliorated oxidative stress by inhibiting intracellular reactive oxygen species (ROS) generation in Hs68 cells. WHS rescued UVB-induced collagen degradation by suppressing MMP expression, and reduced the mRNA levels of inflammatory cytokines. These anti-photoaging activities of WHS were associated with inhibition of the activator protein 1 (AP-1), signal transduction and activation of transcription 1 (STAT1), and mitogen-activated protein kinase (MAPK) signaling pathways. Oral administration of WHS effectively alleviated dorsal skin from wrinkle formation, epidermal thickening, collagen degradation, and skin dehydration in HR-1 hairless mice exposed to UVB. Notably, WHS suppressed UVB activation of the AP-1 and MAPK signaling pathways in dorsal mouse skin tissues. Taken together, our data indicate that WHS prevents UVB-induced skin damage due to collagen degradation and MMP activation via inactivation of MAPK/AP-1 signaling pathway.

Aster glehni (AG) has been used in cooking and as a medicine to treat various diseases for over hundreds of years in Korea. To speculate the protective effects of AG on skin barrier, we estimated the protein levels of biomarkers related to skin barrier protection in human keratinocytes, HaCaT cells treated with sodium dodecyl sulfate (SDS), or 2,4‐dinitrochlorobenzene (DNCB). The protein levels for keratin, involucrin, defensin, tumor necrosis factor alpha (TNFα), peroxisome proliferator‐activated receptor delta (PPARδ), 5′ adenosine monophosphate‐activated protein kinase (AMPK), serine palmitoyltransferase long chain base subunit 2 (SPTLC2), and transient receptor potential cation channel subfamily V member 4 (TRPV4) were evaluated using western blotting or immunocytochemistry in HaCaT cells. AG extract increased the protein levels of PPARδ, phosphorylated AMPK, SPTLC2, keratin, involucrin, and defensin compared to the SDS or DNCB control group. However, TNFα expression increased by SDS or DNCB was decreased with AG extract. The order of action of each regulatory biomarker in AG pathway was identified TRPV4→PPARδ→AMPK from antagonist and siRNA treatment studies. AG can ameliorate the injury of keratinocytes caused by SDS or DNCB through the sequential regulation of TRPV4→PPARδ→AMPK pathway.

Aster glehniis well known for its therapeutic properties. This study was performed to investigate the effects ofA. glehnion nonalcoholic fatty liver disease (NAFLD) in atherosclerotic condition, by determining the levels of biomarkers related to lipid metabolism and inflammation in serum, liver, and adipose tissue. Body and abdominal adipose tissue weights and serum triglyceride level decreased in all groups treated withA. glehni. Serum adiponectin concentration and protein levels of peroxisome proliferator-activated receptorδ, 5′ adenosine monophosphate-activated protein kinase, acetyl-CoA carboxylase, superoxide dismutase, and PPARγcoactivator 1-alpha in liver tissues increased in the groups treated withA. glehni. Conversely, protein levels of ATP citrate lyase, fatty acid synthase, tumor necrosis factorα, and 3-hydroxy-3-methylglutaryl-CoA reductase and the concentrations of interleukin 6 and reactive oxygen species decreased uponA. glehni. Triglyceride concentration in the liver was lower in mice treated withA. glehnithan in control mice. Lipid accumulation in HepG2 and 3T3-L1 cells decreased uponA. glehnitreatment; this effect was suppressed in the presence of the PPARδantagonist, GSK0660. Our findings suggest thatA. glehniextracts may ameliorate NAFLD through regulation of PPARδ, adiponectin, and the related subgenes.